miR-940 regulates the inflammatory response of chondrocytes by targeting MyD88 in osteoarthritis

Osteoarthritis (OA) has been identified to be one of the most prevalent forms of joint disorders, marked with inflammatory immune response that may give rise to several complications including disability. Numbers of investigations have proven that microRNA play a key role in chondrogenesis regulation. Accordingly, the current study was intended to explore more about the potential role of miR-940 in the regulation of immune response, pertaining to osteoarthritis. Our findings indicated miR-940 associated down-regulation in both, the tissue as well as at cellular levels, i.e. chondrocytes that are being induced with IL-1 beta. However, the expression of MyD88 was found to be opposite. Moreover, our findings indicated that miR-940 targets MyD88 to regulate its expression. The study was based on the proposition that normal human chondrocytes when induced with IL-1 beta significantly enhanced the level of inflammation along with simultaneous stimulation of NF-kappa B signaling mechanism. Alternatively, siRNA against MyD88, miR-940 mimic or the NF-kappa B inhibitor, reversed the effect of IL-1 beta. The chondrocytes that were transfected with miR-940 inhibitor increased the secretion of inflammatory cytokines and activated NF-kappa B. Furthermore, the expression of miR-490 was reduced in vivo, which was increased through an injection of lentivirus, to foster the production of necessary cytokines and NF-kappa B and the down-regulation of MyD88. In conclusion, the pathogenesis of OA can be regulated by miR-940/MyD88 axis, which can be achieved through the combined signaling mechanism of MyD88/NF-kappa B signaling, induced with the help of IL-1 beta.